Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Risk factors for a poor early outcome of surgery for stable angina pectoris were evaluated in 2659 consecutive patients from a defined population. The total operative mortality (death within 30 days after surgery) was 2.6% and the frequency of myocardial injury (increase in S-ASAT to greater than 2.0 mu kat l-1 and in S-CKMB to greater than 1.5 mu kat l-1 within 48 h postoperatively or death in the operating room) 14%. Mortality was related to New York Heart Association (NYHA) classification (P less than 0.001), age (less than or greater than 70 years, P = 0.001), duration of symptoms (less than or greater than 8 years, P = 0.001), aortic cross-clamp (ACC) time (P less than 0.001), and cardiopulmonary bypass (CBP) time (P less than 0.001). A multivariate analysis showed that the combination of NYHA class, ACC time and age best predicted operative mortality. Myocardial injury was related to NYHA functional class (P less than 0.001), duration of symptoms (P less than 0.001), regrafting procedure (P less than 0.001), cardiac related dyspnoea (P = 0.015), ACC time (P = 0.001), CPB time (P = 0.001), relative volume of cardioplegic solution (P less than 0.001), and thromboendarterectomy procedure (P = 0.004). The set of variables that best predicted myocardial injury consisted of ACC time, relative volume cardioplegic solution, NYHA class, regrafting procedure and duration of symptoms. However, these risk factors indicated only moderately high risks, and high-risk patients could not be selected with sufficient accuracy.
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PMID:Risk factors for operative mortality and morbidity in patients undergoing coronary artery bypass surgery for stable angina pectoris. 204 49

All cases of coronary bypass procedures without concomitant heart valve replacement occurring in a defined geographical area over a 8-year period (1980-1987) were reviewed and the 30-day mortality and complication rates associated with them were analyzed. The study comprised 3,484 patients with the diagnoses: stable (2477) or unstable (724) angina pectoris, angina pectoris combined with left ventricular aneurysm (165) or with an other complicating factor (96), postinfarction septal defect (13) and postinfarction mitral valve insufficiency (9). The total operative mortality during the study period was 3.1%. Persistent new Q waves in the electrocardiogram developed in 2.4% and increased enzyme release indicating myocardial injury (S-ASAT greater than 2.0 microkat/L and S-CKMB isoenzyme greater than 1.5 microkat/L) occurred in 15%. There were 478 complications in 378 patients (11%). Indication for surgery, year of surgery, NYHA class, congestive heart failure, age, sex, aortic cross-clamp time, and cardiopulmonary bypass time were significantly related to operative mortality (p less than 0.05). The same variables except sex were related to complications. Myocardial infarction (new persistent Q wave) was predictable by NYHA class, aortic cross-clamp time, and cardiopulmonary bypass time. The same variables and also year of surgery, regrafting procedure, congestive heart failure, and thromboendarterectomy were predictors of myocardial injury (enzyme release).
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PMID:Predictive value of factors affecting early results and complications in eight years of coronary artery bypass surgery. 261 1

1306 men less than 68 years of age who survived a first myocardial infarction (MI) during 1968-1977 were followed up between 2 and 12 years. The mean follow-up time was 6.5 years. The patients were unselected and paid regular visits to a Post-MI Clinic where treatment was standardized. The autopsy rate was high and the follow-up of endpoints was complete. The diagnosis of a non-fatal reinfarction was based on conventional clinical criteria, and the diagnosis of a fatal reinfarction on autopsy findings of a recent myocardial injury and/or a fresh coronary thrombus. The patients were randomly assigned to two halves. One was used only for derivation of the predictive models, and the other only for validation. Common clinical variables judged to be prognostically important were selected. Among variables available at discharge from hospital a history of hypertension, angina pectoris or diabetes before the MI and the maximal serum ASAT during the MI were independently related to reinfarctions during the follow-up. A predictive index was formed and validated. The rate of reinfarction among risk quartiles in the validation sample increased from 24 to 38% (P = 0.003). The aetiologic fraction (the percent of reinfarctions predicted by the index) was 24%. Among variables from the follow-up only cessation of smoking after the MI had independent predictive power. A new predictive index including this variable was formed and validated. The reinfarction rate in the risk quartiles increased from 15 to 39% (P less than 0.001). The aetiologic fraction was 44%. When only reinfarctions occurring before the median follow-up time of 21 months were considered, the aetiologic fraction was 62%.
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PMID:Recurrent myocardial infarction. 2. Possibilities of prediction. 402 86

A monoclonal enzyme immunoassay for measuring human ventricular myosin light chain isotype 1 (HVMLC1) in serum has been developed. To evaluate the method in patients with suspected myocardial injury, we studied 51 patients (16 acute myocardial infarction (AMI), 19 unstable angina pectoris (UAP), 9 stable angina pectoris, 3 nonischemic heart disease, 4 hip surgery patients), and 190 controls (blood donors). Serial blood-samples were drawn from patients; a single blood-sample from controls. The diagnostic value of the HVMLC1 assay was compared with total creatine kinase (CK), CKMB activity, CKMB mass concentration, lactate dehydrogenase isoenzyme 1 (LD1), troponin T (TnT) and mitochondrial-aspartate aminotransferase (m-ASAT). The detection limit of HVMLC1 was 0.4 microgram/l (linear range 0-20 micrograms/l). Sera from 190 reference persons did not contain detectable levels of HVMLC1 (< 0.4 microgram/l; 99% percentile). The coefficients of variation were 13% (1.0 microgram/l) and 3.1% (17.7 micrograms/l). Cross-reactivity with myosin from skeletal muscle was seen. Times to peak value were: CK 19.3 +/- 2.0, LD1 43.4 +/- 3.2, HVMLC1 72.9 +/- 7.0, and m-ASAT 67.3 +/- 5.6 h. Time-curves of HVMLC1 and m-ASAT were similar, whereas time-curves for HVMLC1 and TnT were quite different in most cases. Peak value of HVMLC1 was five times higher than CK peak value and eight times that of LD1. HVMLC1 appeared in the blood within hours after the onset of chest pain and in the majority remained for more than a week after AMI. Among patients with UAP 16% (3/19) had elevated HVMLC1 in serum, whereas elevated TnT was seen in 26% (5/19) and elevated CKMB mass in 26% (5/19). We conclude that the new HVMLC1 assay offers a sensitive diagnosis of myocardial injury. It is characterized by a wide diagnostic time window. The similarity of the HVMLC1 and m-ASAT curves indicates that it may be used to estimate the extent of myocardial necrosis.
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PMID:Human ventricular myosin light chain isotype 1 as a marker of myocardial injury. 817 43